AustralieFrV1, Main, Exploration, bibRecord, 00B999

Mechanism of Measles Virus–Induced Suppression of Inflammatory Immune Responses

Identifieur interne : 00B999 ( Main/Exploration ); précédent : 00B998; suivant : 00BA00

Mechanism of Measles Virus–Induced Suppression of Inflammatory Immune Responses

Auteurs : Julien C. Marie [France] ; Jeanne Kehren [France] ; Marie-Claude Trescol-Biémont [France] ; Alexey Evlashev [France] ; Hélène Valentin [France] ; Thierry Walzer [France] ; Rosine Tedone [France] ; Bruce Loveland [Australie] ; Jean-François Nicolas [France] ; Chantal Rabourdin-Combe [France] ; Branka Horvat [France]

Source :

Immunity [ 1074-7613 ] ; 2001.

RBID : ISTEX:1EE2E448B00A1E3E53C7B93755CD449A4E27250C

Descripteurs français

Wicri :
- topic : Vaccin.

English descriptors

Abstract

Abstract: Measles virus (MV) causes profound immunosuppression, resulting in high infant mortality. The mechanisms are poorly understood, largely due to the lack of a suitable animal model. Here, we report that particular MV proteins, in the absence of MV replication, could generate a systemic immunosuppression in mice through two pathways: (1) via MV-nucleoprotein and its receptor FcγR on dendritic cells; and (2) via virus envelope glycoproteins and the MV-hemagglutinin cellular receptor, CD46. The effects comprise reduced hypersensitivity responses associated with impaired function of dendritic cells, decreased production of IL-12, and the loss of antigen-specific T cell proliferation. These results introduce a novel model for testing the immunosuppressive potential of anti-measles vaccines and reveal a specific mechanism of MV-induced modulation of inflammatory reactions.

Url:

https://api.istex.fr/document/1EE2E448B00A1E3E53C7B93755CD449A4E27250C/fulltext/pdf

DOI: 10.1016/S1074-7613(01)00090-5

Affiliations:

Links toward previous steps (curation, corpus...)

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to stream Istex, to step Curation: 000584
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Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Active fragments</term>
<term>Atopic dermatitis</term>
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<term>Cellular immunity</term>
<term>Cellular receptor</term>
<term>Chimeric measles viruses</term>
<term>Contact hypersensitivity</term>
<term>Contact sensitivity</term>
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<term>Dnfb</term>
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<term>Flow cytometry</term>
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<term>Immune response</term>
<term>Immune responses</term>
<term>Immunol</term>
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<term>Immunosuppressive</term>
<term>Immunosuppressive effect</term>
<term>Important role</term>
<term>Independent experiments</term>
<term>Inflammatory</term>
<term>Inflammatory reactions</term>
<term>Inflammatory responses</term>
<term>Inhibitory effect</term>
<term>Intracellular cytokines</term>
<term>Intracellular production</term>
<term>Intracellular staining</term>
<term>Lymph</term>
<term>Lymph nodes</term>
<term>Lymphocyte</term>
<term>Measles</term>
<term>Measles envelope glycoproteins</term>
<term>Measles infection</term>
<term>Measles virus</term>
<term>Measles virus infection</term>
<term>Measles virus proteins</term>
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<term>Node</term>
<term>Normal mice</term>
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<term>Prospective study</term>
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<term>Receptor slam</term>
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<term>Regional lymph nodes</term>
<term>Replication</term>
<term>Respiratory syncytial virus</term>
<term>Sample identity</term>
<term>Sensitization phase</term>
<term>Similar results</term>
<term>Single injection</term>
<term>Subcutaneous injection</term>
<term>Therapeutic efficacy</term>
<term>Third experimenter</term>
<term>Transgenic</term>
<term>Transgenic mice</term>
<term>Transgenic mice ubiquitously</term>
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<term>Vaccine</term>
<term>Ventral skin</term>
<term>Vesicular stomatitis virus</term>
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<term>Virol</term>
<term>Virus</term>
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<keywords scheme="Teeft" xml:lang="en"><term>Active fragments</term>
<term>Atopic dermatitis</term>
<term>Cell population</term>
<term>Cell proliferation</term>
<term>Cell suspensions</term>
<term>Cellular immunity</term>
<term>Cellular receptor</term>
<term>Chimeric measles viruses</term>
<term>Contact hypersensitivity</term>
<term>Contact sensitivity</term>
<term>Critical role</term>
<term>Dendritic</term>
<term>Dendritic cells</term>
<term>Different time points</term>
<term>Dnfb</term>
<term>Edmonston strain</term>
<term>Effector</term>
<term>Effector phase</term>
<term>Envelope proteins</term>
<term>Flow cytometry</term>
<term>Footpad</term>
<term>Glycoprotein</term>
<term>Horvat</term>
<term>Human dendritic cells</term>
<term>Hypersensitivity</term>
<term>Hypersensitivity reactions</term>
<term>Hypersensitivity responses</term>
<term>Immune</term>
<term>Immune response</term>
<term>Immune responses</term>
<term>Immunol</term>
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<term>Immunosuppressive</term>
<term>Immunosuppressive effect</term>
<term>Important role</term>
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<term>Inflammatory responses</term>
<term>Inhibitory effect</term>
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<term>Intracellular production</term>
<term>Intracellular staining</term>
<term>Lymph</term>
<term>Lymph nodes</term>
<term>Lymphocyte</term>
<term>Measles</term>
<term>Measles envelope glycoproteins</term>
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<term>Measles virus</term>
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<term>Normal mice</term>
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<term>Prospective study</term>
<term>Receptor</term>
<term>Receptor slam</term>
<term>Recombinant</term>
<term>Regional lymph nodes</term>
<term>Replication</term>
<term>Respiratory syncytial virus</term>
<term>Sample identity</term>
<term>Sensitization phase</term>
<term>Similar results</term>
<term>Single injection</term>
<term>Subcutaneous injection</term>
<term>Therapeutic efficacy</term>
<term>Third experimenter</term>
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<front><div type="abstract" xml:lang="en">Abstract: Measles virus (MV) causes profound immunosuppression, resulting in high infant mortality. The mechanisms are poorly understood, largely due to the lack of a suitable animal model. Here, we report that particular MV proteins, in the absence of MV replication, could generate a systemic immunosuppression in mice through two pathways: (1) via MV-nucleoprotein and its receptor FcγR on dendritic cells; and (2) via virus envelope glycoproteins and the MV-hemagglutinin cellular receptor, CD46. The effects comprise reduced hypersensitivity responses associated with impaired function of dendritic cells, decreased production of IL-12, and the loss of antigen-specific T cell proliferation. These results introduce a novel model for testing the immunosuppressive potential of anti-measles vaccines and reveal a specific mechanism of MV-induced modulation of inflammatory reactions.</div>
</front>
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Mechanism of Measles Virus–Induced Suppression of Inflammatory Immune Responses

Mechanism of Measles Virus–Induced Suppression of Inflammatory Immune Responses

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Descripteurs français

English descriptors

Abstract

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